Diagnostic agent for parkinson's disease

Abstract

The present invention relates to method of identifying whether or not an individual has Parkinson's disease (PD). In particular, the invention relates to a method for identifying whether or not an individual has PD in the pre-symptomatic phase of the disease or to distinguishing PD from another neurological disorder. The method of the invention comprises measuring the amount of soluble α-synuclein oligomers in a cerebrospinal fluid sample taken from an individual. The method optionally also comprises measuring the total amount of α-synuclein in the CSF sample, calculating the ratio of the amount of α-synuclein oligomers to the total amount of α-synuclein, and thereby determining whether or not the individual has PD. The method of the invention can be used in clinical trials to measure the effect of drugs in both PD animal models and human PD patients.

Description

FIELD OF THE INVENTION[0001]The present invention relates to method of identifying whether or not an individual has Parkinson's disease (PD). In particular, the invention relates to a method for identifying whether or not an individual has PD in the pre-symptomatic phase of the disease.BACKGROUND OF THE INVENTION[0002]Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease. The earliest clinical features of PD are typically identified retrospectively and are not specific for PD. These symptoms are typically non-motor symptoms such as constipation, depression, hyposmia, and sleep disorders.[0003]The more generally recognised symptoms of PD are motor symptoms such as bradykinesia, muscle tremor, rigidity and balance problems. These symptoms do not appear until much later in the disease, when major damage to the brain has already occurred. Indeed, at least 70% of nigral neurons in the midbrain must be lost prior to the appearance of sympt...

AI Technical Summary

Benefits of technology

[0007]The discovery of mutations in the gene encoding α-synuclein (SNCA) in familial cases of PD first suggested a critical role for α-synuclein (α-syn) protein in the etiology of idiopathic PD. More recently, genetic studies have also revealed that rare triplication events in SNCA can be associated with severe forms of young-onset, familial PD that also feature dementia with Lewy body-type changes. Furthermore, duplication mutations cause a familial PD phenotype that more closely resembles late-onset, idiopathic PD. These collective studies indicate that an increased expression of wild-type α-syn enhances the risk of developing PD and that the protein level of α-syn might be an important determinant of the progression and severity of the Parkinsonian phenotype.

Problems solved by technology

Even then, the first manifestation of motor symptoms may be subtle and can go unnoticed for months or years.

Accurate clinical diagnosis of PD during life is highly difficult, being correct in only about 85% of cases.

As a consequence, the discovery of effective disease-modifying therapies has been impeded.

These methods are costly and it remains a matter of debate how closely they reflect the underlying pathologic process.

To date, there is no test which can reliably determine whether or not an individual has PD.

In particular, there is no test which can determine whether or not an individual has PD during the early (pre-symptomatic) phase of the disease, before too much damage to the brain has occurred.

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